Reduced osteoclast-derived apoptotic bodies in bone marrow characterizes the pathological progression of osteoporosis

[1]  R. Chen,et al.  Ghost messages: cell death signals spread , 2023, Cell Communication and Signaling.

[2]  N. Salari,et al.  The global prevalence of osteoporosis in the world: a comprehensive systematic review and meta-analysis , 2021, Journal of Orthopaedic Surgery and Research.

[3]  W. Lems,et al.  Bone Mineral Density Loss and Fracture Risk After Discontinuation of Anti-osteoporotic Drug Treatment: A Narrative Review , 2021, Drugs.

[4]  Yongguang Gao,et al.  The Development of Molecular Biology of Osteoporosis , 2021, International journal of molecular sciences.

[5]  J. Kemp,et al.  Osteoclasts recycle via osteomorphs during RANKL-stimulated bone resorption , 2021, Cell.

[6]  F. Luo,et al.  Osteoclast-derived apoptotic bodies couple bone resorption and formation in bone remodeling , 2021, Bone Research.

[7]  J. Xing,et al.  Osteoclast-derived apoptotic bodies show extended biological effects of parental cell in promoting bone defect healing , 2020, Theranostics.

[8]  Zhousheng Xiao,et al.  Osteoporosis: Mechanism, Molecular Target, and Current Status on Drug Development. , 2020, Current medicinal chemistry.

[9]  Yun Bai,et al.  Mature osteoclast–derived apoptotic bodies promote osteogenic differentiation via RANKL-mediated reverse signaling , 2019, The Journal of Biological Chemistry.

[10]  M. Haris,et al.  Extracellular vesicles-mediated intercellular communication: roles in the tumor microenvironment and anti-cancer drug resistance , 2019, Molecular Cancer.

[11]  A. Infante,et al.  Osteogenesis and aging: lessons from mesenchymal stem cells , 2018, Stem Cell Research & Therapy.

[12]  Y. Tabata,et al.  Coupling of bone resorption and formation by RANKL reverse signalling , 2018, Nature.

[13]  S. Shi,et al.  Circulating apoptotic bodies maintain mesenchymal stem cell homeostasis and ameliorate osteopenia via transferring multiple cellular factors , 2018, Cell Research.

[14]  I. Poon,et al.  Apoptotic Cell-Derived Extracellular Vesicles: More Than Just Debris , 2018, Frontiers in Immunology.

[15]  S. Papapoulos,et al.  Paget's disease of bone. , 2001, Best practice & research. Clinical endocrinology & metabolism.

[16]  S. Khosla,et al.  Osteoporosis treatment: recent developments and ongoing challenges. , 2017, The lancet. Diabetes & endocrinology.

[17]  S. Teitelbaum.  Therapeutic implications of suppressing osteoclast formation versus function. , 2016, Rheumatology.

[18]  H. Valadi,et al.  Extracellular Vesicles: Evolving Factors in Stem Cell Biology , 2015, Stem cells international.

[19]  Leonora Balaj,et al.  Extracellular Vesicles: Composition, Biological Relevance, and Methods of Study. , 2015, Bioscience.

[20]  S. Mathivanan,et al.  A novel mechanism of generating extracellular vesicles during apoptosis via a beads-on-a-string membrane structure , 2015, Nature Communications.

[21]  M. Kerachian,et al.  Role of apoptosis in pathogenesis and treatment of bone-related diseases , 2015, Journal of Orthopaedic Surgery and Research.

[22]  A. Schulz,et al.  Osteopetrosis: genetics, treatment and new insights into osteoclast function , 2013, Nature Reviews Endocrinology.

[23]  M. Olson,et al.  Blebs produced by actin–myosin contraction during apoptosis release damage-associated molecular pattern proteins before secondary necrosis occurs , 2013, Cell Death and Differentiation.

[24]  Imre Mäger,et al.  Extracellular vesicles: biology and emerging therapeutic opportunities , 2013, Nature Reviews Drug Discovery.

[25]  Graça Raposo,et al.  Extracellular vesicles: Exosomes, microvesicles, and friends , 2013, The Journal of cell biology.

[26]  S. Khosla,et al.  Estrogen and the skeleton , 2012, Trends in Endocrinology & Metabolism.

[27]  C. Dinarello,et al.  Sterile inflammation of endothelial cell-derived apoptotic bodies is mediated by interleukin-1α , 2011, Proceedings of the National Academy of Sciences.

[28]  T. Rachner,et al.  Osteoporosis: now and the future , 2011, The Lancet.

[29]  M. Hristov,et al.  Delivery of MicroRNA-126 by Apoptotic Bodies Induces CXCL12-Dependent Vascular Protection , 2009, Science Signaling.

[30]  David L. Lacey,et al.  Osteoclast differentiation and activation , 2003, Nature.

[31]  Lars Holmgren,et al.  Horizontal transfer of oncogenes by uptake of apoptotic bodies , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[32]  T. Martin,et al.  Therapeutic approaches to bone diseases. , 2000, Science.

[33]  S. Teitelbaum,et al.  Bone resorption by osteoclasts. , 2000, Science.

[34]  S. Manolagas,et al.  Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. , 2000, Endocrine reviews.

[35]  T. Yoneda,et al.  Bisphosphonates promote apoptosis in murine osteoclasts in vitro and in vivo , 1995, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[36]  A. Steinberg.  MRL-lpr/lpr disease: theories meet Fas. , 1994, Seminars in immunology.

[37]  Claus Christiansen,et al.  Diagnosis of Osteoporosis , 1992, Southern medical journal.

[38]  H. DeLuca.  Vitamin D endocrinology. , 1976, Annals of internal medicine.